|Year : 2018 | Volume
| Issue : 1 | Page : 23-27
Can smoking affect cognition in bipolar patients?
Heba Aly1, Hoda Salama2, Soha Ibrahim2, Hesham Shestawy2
1 Department of Psychiatry, El Maamoura Mental Hospital, Faculty of Medicine, Alexandria University, Alexandria, Egypt
2 Department of Neuropsychiatry, Faculty of Medicine, Alexandria University, Alexandria, Egypt
|Date of Submission||07-Sep-2017|
|Date of Acceptance||10-Oct-2017|
|Date of Web Publication||29-Jan-2018|
Department of Neuropsychiatry, Faculty of Medicine, Alexandria University, Alexandria, 21525
Source of Support: None, Conflict of Interest: None
Background Smoking is highly prevalent in bipolar patients. In addition, cognitive dysfunctions are reported in most of the bipolar patients even in remission state. Does this mean that smoking can affect cognition in bipolar patients similar to what is hypothesized in schizophrenic patients?
Objective The objective of this research was to study the correlation between smoking and cognitive dysfunction in bipolar patients.
Participants and methods A total of 150 bipolar patients (50 manic, 50 depressed, and 50 euthymic) in Maamoura Hospital were compared with 50 controls regarding smoking, Hamilton Depression Rating Scale, Young Mania Rating Scale, and cognitive functions using Wisconsin Card Sorting Test and digit span test and digit symbol test.
Results The percentage of smoking was significantly higher in all patients’ groups compared with the control group. No statistically significant relations were found between performance on the Wisconsin Card Sorting Test-128, digit span neither forward nor backward digit span subtest of the Wechsler Adult Intelligence Scale − Revised (WAIS-R), the digit symbol substitution test (the digit symbol subtest of the WAIS-R) and smoking in manic, depressed, and control groups. A statistically significant positive relation was found between performance of the euthymic patients in forward digit span subtest of the WAIS-R and smoking.
Conclusion Smoking may have a positive effect on sustained attention of bipolar patients during euthymic state, but not in active illness state. Further research is needed to disclose how we can exploit the beneficial cognitive effect of nicotine by avoiding the deleterious effect of tobacco smoking.
Keywords: bipolar, cognition, smoking
|How to cite this article:|
Aly H, Salama H, Ibrahim S, Shestawy H. Can smoking affect cognition in bipolar patients?. Egypt J Psychiatr 2018;39:23-7
| Introduction|| |
Cigarette smoking is very prevalent in bipolar disorder (Waxmonsky et al., 2005; Heffner et al., 2008). Patients suffering from bipolar disorders usually die three decades earlier than the general population (Colton and Manderscheid, 2006). Most of these deaths are due to cancer, cardiovascular causes, and respiratory causes. All the previous mentioned causes are related to cigarette smoking (United States Department of Health and Human Services, 2004). Despite these bad implications of smoking, researches in this area are limited (Heffner et al., 2011; Thomson et al., 2015).
It is now believed that most of the bipolar patients have only partial remission from mood and cognitive symptoms in between the episodes (Judd et al., 2002; Judd et al., 2003; Daban et al., 2006; Robinson et al., 2006; Torres et al., 2007; Arts et al., 2008; Kurtz and Gerraty, 2009).
It is well observed that smoking is highly prevalent in schizophrenia. Some studies points at the improvement of some cognitive functions in smoker schizophrenic patients, considering smoking as a ‘self-medication’ (Dépatie et al., 2002; Sacco et al., 2004; Kumari and Postma, 2005; Sacco et al., 2005; Beck et al., 2015).
Smoking is highly prevalent in bipolar patients. Also, cognitive dysfunctions are reported in most of the bipolar patients even in remission state. Does this mean that smoking can affect cognition in bipolar patients similar to what is hypothesized in schizophrenic patients?
| Aim|| |
The aim of this work is to study the correlation between smoking and cognitive dysfunction in bipolar patients.
| Participants and methods|| |
This study was conducted in 150 persons (100 bipolar patients receiving treatment either as inpatients or outpatients in El Maamora Psychiatric Hospital compared with 50 matched controls). Informed written consent was taken from each patient to participate in this study. The sample was collected randomly with the following inclusion and exclusion criteria:
The inclusion criteria were as follows:
- Diagnoses: bipolar disorder according to Diagnostic and Statistical Manual of Mental Disorders, 4th ed., text revision (DSM-IV TR) criteria (American Psychiatric Association, 2000) − manic (38 patients), depressed (26 patients), and bipolar in remission (36 patients).
- Age: 18–50 years.
- Informed written consent was taken from each patient to participate in this study.
The exclusion criteria were as follows:
- Other psychiatric disorders.
- History of substance dependence in the past year.
- History of electroconvulsive therapy in the past year.
- Chronic physical or neurological debilitating disorders especially those affecting cognition − for example, endocrine disorders, Parkinson’s disease.
All patients were evaluated using the following tools:
- Clinical psychiatric interview (with special emphasis on cigarette smoking).
- Psychometric studies:
- Hamilton Depression Rating Scale.
- Young Mania Rating Scale.
- Cognitive function assessment was done using the following psychometric tests:
- The Wisconsin Card Sorting Test is a standard test used to assess working memory and executive functions (Heaton, 1993).
- Digit span test was used to evaluate short-term memory, as well as attention and concentration (Meleika, 1996).
- Digit symbol was used to assess visual motor speed and perception (Meleika, 1996).
| Results|| |
Regarding sex, there was no statistically significant difference between the four groups (P>0.05). The manic patients’ group included 19 (50.0%) men and 19 (50.0%) women, the depressed patients’ group included 12 (46.2%) men and 14 (53.8%) women, the euthymic patients’ group included 20 (55.6%) men and 16 (44.4%) women, and the control group included 25 (50.0%) men and 25 (50.0%) women.
Regarding age, there was no statistically significant difference between the four groups (P>0.05). The manic patients’ age ranged between 22 and 50 years with a mean of 35.42±8.43, the depressed patients’ age ranged between 18 and 50 years with a mean of 35.85±9.32, the euthymic patients’ age ranged between 23 and 49 years with a mean of 37.8±7.38, and the control age ranged between 21 and 50 years with a mean of 34.92±7.76.
Regarding smoking, the number of smoker manic patients − 20 (52.6%) smokers − was significantly higher than the number of smokers in the control group − five (10.0%) smokers (P<0.001). On the other hand, the number of smoker depressed patients [11 (42.3%) smokers] was significantly higher than the number of smokers in control group [five (10.0%) smokers] (P≤0.05). The number of smoker euthymic patients [16 (44.4%) smokers] was significantly higher than the number of smokers in the control group [five (10.0%) smokers] (P<0.001). There was no statistically significant difference between the euthymic patients and the other two groups (the manic and the depressed patients) or between the manic and the depressed patients ([Figure 1]).
|Figure 1 Percentage of smokers among the manic, the depressed, the euthymic patients, and the control groups.|
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The relation between smoking and performance of studied groups in the cognitive psychometric tests is shown in [Table 1]:
|Table 1 The relation between smoking and performance of the manic, the depressed, the euthymic patients, and the control groups in the cognitive psychometric tests|
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Regarding the manic, the depressed, and the control groups, no statistically significant relations were found between performance on the Wisconsin Card Sorting Test-128, digit span neither forward nor backward digit span subtest of the Wechsler Adult Intelligence Scale − Revised (WAIS-R), the digit symbol subtest of the WAIS-R, and smoking. On the other hand, a statistically significant positive relation was found between performance of the euthymic patients in forward digit span subtest of the WAIS-R and smoking.
| Discussion|| |
It is well known that cigarette smoking is a definite risk factor for many hazardous illnesses. However, many studies reported the beneficial effect of smoking in schizophrenia (Dépatie et al., 2002; Sacco et al., 2004; Kumari and Postma, 2005; Sacco et al., 2005; Beck et al., 2015). Is this finding the same in bipolar disorder?
In the current study, cigarette smoking in patients’ groups was significantly higher than in the control group. The percentage of smoking was 52.6, 42.3, 44.4, and 10% in manic, depressed, euthymic, and control groups, respectively. There was no statistically significant difference in smoking percentages among patients’ groups. This finding is consistent with what was found in previous studies. These studies showed that cigarette smoking was approximately two to three times more prevalent in bipolar disorder than in the general population. Cigarette smoking percentage was 60–70% in bipolar patients compared with 25–30% in the general population (Lasser et al., 2000; Heffner et al., 2011; Ng et al., 2014).
What is the association between cigarette smoking and bipolar disorder? Different theories tried to explain this association. For example, nicotine in tobacco is said to cause release of dopamine and norepinephrine that are implicated in pathophysiology of bipolar disorder and also thought to play a role in addiction (Stockings et al., 2013). Another supposed mechanism is that activity of monoamine oxidase enzyme is reduced in smokers. This leads to an increase of dopamine and serotonin, which are implicated in pathology of bipolar disorder (Stockings et al., 2013). Glutamate is another neurotransmitter that is said to have a role in pathophysiology of mood disorders (Zarate et al., 2006; Phelps et al., 2009; aan het Rot et al., 2010; Diazgranados et al., 2010). Nicotine is said to have a modulating effect on glutamate in synapses of nucleus accumbens (Kalivas, 2009; Brown et al., 2013). This relation between nicotine and glutamate can be involved in drug relapse (Gipson et al., 2014).
In the current study, smoking did not affect (neither improved nor worsened) tested cognitive functions in manic, depressed, and control groups. On the other hand, in euthymic group, smokers were significantly better than nonsmokers in forward digit span subtest of the WAIS-R. This means that smoking can improve the selective attention in euthymic bipolar patients, but has no effect during active illness (manic or depressive episodes).
Beck et al. (2015) studied the effect of smoking (active or abstinent) on putative three endophenotypic markers in schizophrenic patients: visuospatial working memory, continuous performance test identical pairs, and prepulse inhibition. They found that smoker schizophrenic patients perform better than abstinent schizophrenic control as regards visuospatial working memory. However, no significant difference was observed between the smoker and abstinent group in results of continuous performance test identical pairs and prepulse inhibition (Beck et al., 2015).
This can give a hint that smoking can improve some aspects of cognitive functions in bipolar patients ‘specifically in euthymic state’. This can be a shining side of nicotine, hoping to be of therapeutic benefit. The presumed ability of nicotine to improve sustained attention in euthymic state, not in active illness state, may be related to the impairing effect of mood on cognitive processing.
However, the huge black side of smoking must be put in our consideration. Adan et al. (2004) reported low mood scores in highly dependent smokers, intermediate mood scores in low dependent smokers, and high mood scores in nonsmokers. Polycyclic aromatic hydrocarbons in tobacco smoke increase the metabolism of some psychotropic medications via the induction of the hepatic cytochrome P450 enzyme. This leads to lower serum levels of drugs including olanzapine, as well as other antipsychotics, antidepressants, and benzodiazepines. That is why tobacco smoking reduces the therapeutic benefits of taking these medications. Therefore, smokers with bipolar need an increased dose, ∼50% higher, to achieve an adequate therapeutic response (Haslemo et al., 2006). In addition, nicotine’s activation of the sympathetic nervous system may reduce the sedating effects of benzodiazepines (Heffner et al., 2011).
| Conclusion|| |
Smoking may have a positive effect on sustained attention of bipolar patients during euthymic state, but not in active illness state. Further research is needed to disclose how we can exploit the beneficial cognitive effect of nicotine by avoiding the deleterious effect of tobacco smoking.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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